Beruflich Dokumente
Kultur Dokumente
Institute of Molecular Medicine, Faculty of Medicine, University of Lisbon, b Stroke Unit, Neurology Service and
Psychiatry Service, Department of Neurosciences, Hospital de Santa Maria, Faculty of Medicine, University of Lisbon,
Lisbon, Portugal
Key Words
Mania Stroke
Abstract
Background: Mania is a rare consequence of stroke and according to the sparse published information it is difficult to
describe its demographic, clinical and prognostic characteristics. Methods: We performed a systematic review of all cases of mania and stroke to describe those characteristics.
Studies were identified from comprehensive searches of
electronic databases, reference lists of the studies collected
and handbooks. Two authors independently assessed abstracts, and collected and extracted data. Results: From 265
abstracts, 139 were potentially relevant. For the first analysis,
which tries to answer the clinical question of the relationship
between mania and stroke, 49 studies met the inclusion criteria and described 74 cases. For the second analysis, we
looked for an explicit temporal and causal relationship between manic symptoms and stroke, and selected 32 studies
describing 49 cases. In both analyses, the typical patient was
male, without a personal or family history of psychiatric disorder, with at least one vascular risk factor, but without subcortical atrophy and had suffered a right cerebral infarct. The
majority of patients (92%) presented elevated mood as the
first symptom. The other frequent symptoms were an increased rate or amount of speech (71%), insomnia (69%) and
agitation (63%). Conclusions: Post-stroke mania should be
Introduction
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Methods
Search Strategy
Relevant articles on post-stroke mania cases were identified by
electronic search of MEDLINE (until December 2010), by crossreferencing the following MeSH terms: bipolar disorder and
cerebrovascular disease (online suppl. table 1; for all online
suppl. material, see www.karger.com/doi/10.1159/000327032).
We also ran the search in EMBASE and Web of Science databases
and identified other cases and studies consulting the reference list
of the studies collected and handbooks of neuropsychiatry of
stroke. Two authors (C.O.S., J.M.F.) independently assessed all abstracts, and collected and extracted data.
Inclusion Criteria
The primary outcome was the presence of secondary mania
after a stroke. For inclusion, studies were required to fulfil the following inclusion criteria: (1) all cases of mania and stroke, (2) patients with a diagnosis of cerebral infarct, intracerebral haemorrhage or subarachnoid haemorrhage, and (3) adult patients (618
years old).
We performed two different analyses. In the first one, we included all cases of mania and stroke, even when the temporal or
causal relationship (Appendix) between them was not explicit or
did not exist. This analysis answers the clinical question of what
relationship exists between mania and stroke.
In the second analysis, we looked for an explicit temporal and
causal relationship between manic symptoms and stroke. Therefore, we applied DSM-IV-TR criteria of mood disorder due to
acute stroke with manic features [1] and the criteria of secondary
mania by Krauthammer and Klerman [6] (table1).
Exclusion Criteria
Studies that met one of the following items were excluded from
both analyses: (1) duplicate reports; (2) cases with unruptured aneurysms or subdural haematoma, and (3) cases with a diagnosis
of bipolar disorder and/or manic episodes before the index stroke.
Data Extraction
The following general descriptive information was extracted
from each study: (1) type of study: randomized controlled trial,
cohort study, case-control study, case series or case report; (2) diagnosis, diagnostic criteria (DSM or ICD), type of assessment
(clinical and/or mania scales) and interviewer (neurologist, psychiatrist, psychologist, nurse); (3) demography and past medical
history: age, gender, years of education, personal and/or family
history of psychiatric disorder and vascular risk factors; (4) symptoms and signs, onset, duration, description; (5) stroke: type, location and presence of subcortical atrophy on CT/MRI; (6) treat-
12
Results
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18]. Based on the sparse published information, it is difficult to describe the demographic, clinical and prognostic characteristics of post-stroke mania. This systematic
review of all cases of mania associated with stroke published until December 2010 tries to answer those questions and to increase the robustness of the evidence of
this neuropsychiatric complication of stroke.
MeSH TERMS
Bipolar disorder and cerebrovascular disease
Electronic databases
233 articles
Reference lists
22 articles
Handbooks
10 articles
Total number of
studies: 265
SORTING CRITERIA
Primary outcome poststroke mania
139 potentially relevant
INCLUSION CRITERIA
(1) All new cases of mania and stroke reported
(2) Diagnosis of cerebral infarct, intracerebral haemorrhage
or subarachnoid haemorrhage
(3) Adult patients (18 years old)
1ST ANALYSIS
All the cases of mania and stroke
2ND ANALYSIS
Temporal and causal relationship between
manic symptoms and stroke
=
secondary mania (Krauthammer and Klerman
[6]) + mood disorder due to acute stroke with
manic features (DSM-IV-TR)
FINAL SELECTION
49 studies
74 cases
FINAL SELECTION
32 studies
49 cases
least one vascular risk factor, but without subcortical atrophy and had suffered a right cerebral infarct.
In 49 of the 74 cases, we could find a temporal and
causal relationship between stroke and mania. In another 4 cases, mania occurred concomitantly with a change
or initiation of a treatment which might cause mania in
stroke patients with different evolution time periods.
Four patients had had a previous affective disorder; 3 had
depression [20, 28, 30] and 1 cyclothymia [8]. In 17 cases,
we could not determine the relationship between stroke
and mania.
Second Analysis Cases of Secondary Mania
When we only included the 49 patients with poststroke mania, we found similar results to those obtained
in the first analysis (table 5). The typical patient with
post-stroke mania was male, without a personal or family history of psychiatric disorder, with at least one vascular risk factor, without subcortical atrophy and had suffered a right cerebral infarct. In all those cases, there
Cerebrovasc Dis 2011;32:1121
13
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Number of
References
studies (n = 49)
Type of study
Randomized controlled trial
Cohort study
Case-control study
Case series
Case report
Retrospective
0
4
0
7
35
3
Department
Neurology
Psychiatry
Both
Other
Not specified
14
30
3
1
1
16, 29, 34, 3841, 44, 46, 47, 51, 54, 57, 61
7, 8, 12, 1725, 27, 28, 3032, 3537, 42, 43, 45, 48, 50, 52, 55, 58, 59, 60
33, 53, 56
26
49
Diagnosis
DSM criteria
ICD criteria
Krauthammer and Klerman
Not specified
17
3
3
26
12, 16, 17, 20, 2226, 34, 38, 39, 43, 44, 46, 52, 61
8, 27, 50
18, 19, 58
7, 21, 2833, 3537, 4042, 45, 4749, 51, 5357, 59, 60
Type of assessment
Clinical
Scale
Both
Not specified
27
0
17
5
7, 8, 1618, 2022, 24, 26, 3032, 34, 35, 37, 38, 40, 42, 43, 45, 48, 53, 54, 57, 58, 60
12, 19, 23, 25, 27, 28, 29, 33, 36, 39, 41, 44, 46, 47, 52, 56, 61
4951, 55, 59
Interviewer
Medical doctor
Psychiatrist
Psychologist
Nurse
Not specified
1
9
1
0
38
41
12, 22, 23, 29, 31, 38, 43, 52, 60
61
7, 8, 1619, 20, 21, 2428, 30, 3237, 39, 40, 42, 4451, 5359
seemed to be a clear temporal and causal relationship between stroke and mania. The majority of mania cases appeared in the first days after stroke, with 53% immediately after stroke, 23% during the first month after stroke
and 23% after this first month. In the online supplementary table2, we present the description of each case.
Table6 describes the symptoms of mania in those 49
cases. The majority of patients (92%) presented elevated
mood as the first symptom. Forty-one percent of patients
(n = 20) alternated between elevated and irritable mood
and only 8% presented irritability only. The other frequent symptoms were an increased rate or amount of
speech (71%), insomnia (69%) and agitation (63%). We
counted the number of core symptoms of mania and the
majority of patients presented 5 or more symptoms of
mania (31% 56 symptoms and 27% 67 symptoms).
14
Considering the patients for whom we had information, in the majority of these cases mania lasted between
1 and 12 weeks, more frequently without recurrence or
minor symptoms (hypomania).
Treatment of Secondary Mania
Of the 74 cases, we have data on the treatment for only
47 cases (64%). Mood stabilizers (lithium, carbamazepine and valproic acid) were used in 62%, typical antipsychotics (haloperidol) in 32%, atypical antipsychotics
(olanzapine, risperidone) in 19% and benzodiazepines
(diazepam, lorazepam) in 13%. Data on dosages, duration
of the treatment and efficacy were so scarce that it was
impossible to provide any meaningful results.
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Studies characteristics
Criteria
Description
Number of
References
studies (n = 90)
Duplicated reports
Revisions
Description of not new cases
32 (36%)
911, 1315, 62, 64, 6871, 78, 80, 88, 93, 98, 99, 101
104, 107, 109, 110, 112, 114, 117, 125, 128, 132, 137
No stroke
Aneurisms unruptured
Subdural haematoma
No stroke
19 (21%)
63, 65, 72, 73, 77, 79, 81, 84, 86, 100, 106, 121, 124,
126, 130, 131, 133, 135, 142
Previous affective
disorder
Bipolar disorder
Mania
Other neuropsychiatric disturbances
32 (36%)
5, 66, 67, 7476, 82, 83, 85, 87, 89, 91, 92, 94, 95, 97,
105, 108, 113, 115, 116, 118, 120, 122, 123, 127, 129,
134, 136, 138, 140, 141
7 (7%)
This systematic review confirms the rarity of poststroke mania because in about 50 years we found only 74
reported cases of adult stroke patients with mania symptoms. Robinson et al. [10] and Dunne et al. [145] identified only 3 cases of post-stroke mania in a series of 700
and 661 consecutive stroke patients, respectively. Among
188 consecutive acute stroke patients, our group found 3
(1.6%) cases of mania [61]. Although mania can be very
disrupting during hospitalization and recovery, its low
prevalence limits the description of clinical, demographic and prognostic features and the identification of evidence-based strategies for dealing with it.
We found a typical patient to be male, without a personal/family history of psychiatric disorder, with at least
one vascular risk factor, without subcortical atrophy and
with a right cerebral infarct. Our results support previous
research which concludes that there is a significant relationship between post-stroke mania and right hemispheric lesions causing a dysfunction in the ventral limbic
circuit that involves the right orbitofrontal and basotemporal cortices, dorsomedial thalamic nucleus and head of
the caudate nucleus [10, 16, 27, 78, 80]. The orbitofrontal
circuit is a complex functional network that includes the
orbitofrontal cortex, the basotemporal region, the thalamus and the caudate nucleus and is a central circuit in
mood regulation and social behaviour [16, 33].
Establishing a causal relationship between stroke and
mania has also been based on other factors than right lesions. The lack of a previous personal or family psychiatric
affective disorder, the presence of vascular risk factors and
Discussion
15
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Variables
Age
<65
65
Range
No information
Gender
Female
Male
No information
History of personal psychiatric disorder
Yes
No
No information
Family history of psychiatric disorder
Yes
No
No information
Vascular risk factors
Yes
No
No information
Stroke type
Cerebral infarct
Intracerebral haemorrhage
Subarachnoid haemorrhage
No information
Stroke laterality
Right
Left
Bilateral
No information
Subcortical atrophy
Yes
No
No information
Relation with stroke
Causal and temporal relationship
Secondary to treatment
Previous affective disorderc
Unknown
Cases
(n = 63)
35
22
2791
17
0.19a
17
44
13
0.00a
4
55
15
0.00a
3
38
33
0.00a
26
7
41
0.00a
56
7
9
2
0.00b
50
11
4
9
0.00b
2
36
36
0.00a
49
4
4
17
0.00b
Variables
Cases
p
(n = 45)
Age
<65
65
Range
No information
Gender
Female
Male
No information
History of personal psychiatric disorder
Yes
No
No information
Family history of psychiatric disorder
Yes
No
No information
Vascular risk factors
Yes
No
No information
Stroke type
Cerebral infarct
Intracerebral haemorrhage
Subarachnoid haemorrhage
No information
Stroke laterality
Right
Left
Bilateral
No information
Subcortical atrophy
Yes
No
No information
a
b
25
11
2781
13
0.05a
11
28
10
0.01a
1
47
1
0.00a
2
29
18
0.00a
20
7
22
0.02a
36
6
7
0
0.00b
39
7
3
0
0.00b
0
29
20
0.00a
16
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cerebral lesions [16, 60]. Antipsychotics were used in cases of severe mania with psychotic symptoms, and throughout all these years atypical antipsychotics have been preferred because they have comparatively minor side effects.
Benzodiazepines were also used as adjunctive treatment
for hyperactivity and insomnia [32]. These drugs should
be given to post-stroke mania patients with caution for
two main reasons: first because older patients have a high
sensitivity to psychotropic drugs and second because the
presence of stroke itself could change their efficacy [114].
19
24
25
26
26
27
29
31
32
33
34
36
7
38
17
40
41
43
45
46
47
48
12
12
12
12
12
12
12
12
12
12
51
51
52
52
52
52
52
53
56
57
16
16
18
18
58
60
61
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
Total
45
Irritability
Hyperactivity
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
TalkDistract- Flight
ativeness ibility
of ideas
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
24
31
35
13
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
Sleeplessness
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
Grandiosity
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
Denial
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
x
21
20
34
15
Symptoms, n
Duration Followweeks
up
3
7
8
6
6
6
6
6
9
7
7
3
7
8
7
3
4
6
6
7
6
7
12
4
4
6
6
3
3
3
4
6
3
6
7
7
5
6
5
9
Recurrence
y
y
n
hypomania
12
4
y
y
n
hypomania
8
8
10
8
hypomania
y
y
y
n
8
8
4
38
48
52
cyclic
y
y
n
n
y
y
y
y
n
n
y
y
y
y
y
y
n
18
cyclic
8
4
6
cyclic
cyclic
2
17
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Ref.
Appendix
Temporal or causal relationship = there is evidence from historical data, physical examination, or laboratory findings that
manic symptoms are a direct physiological consequence of a
stroke, occurring immediately or up to 3 years thereafter.
History of personal psychiatric disorder = previous psychiatric
disorder was diagnosed if the patient had at least once in his/her
lifetime been treated for a psychiatric disorder and specific medication for this condition had been prescribed for more than a
month.
Family history of psychiatric disorder = presence of psychiatric
disorder diagnosed in family relatives.
Vascular risk factors = includes hypertension, diabetes mellitus, hyperlipidaemias, myocardial infarction, angina pectoris,
heart failure, atrial fibrillation, lower limb arteriopathy and peripheral vascular disease, history of stroke and/or transient ischaemic attack; cigarette smoking and alcohol consumption.
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